Cognitive deficits associated with a high-fat diet and insulin resistance are potentiated by overexpression of ecto-nucleotide pyrophosphatase phosphodiesterase-1. Issue 64 (February 2018)

• Record Type: Journal Article
• Authors: Kasper, J.M.; Milton, A.J.; Smith, A.E.; Laezza, F.; Taglialatela, G.; Hommel, J.D.; Abate, N.
• Is Part Of: International journal of developmental neuroscience. Issue 64(2018:Feb.)
• Page Start: 48
• Page End: 53
• Publication Date: 2018-02
• Subjects: Developmental neurobiology -- Periodicals; Neurology -- Periodicals; Neurologie du développement -- Périodiques; Developmental neurobiology; Periodicals; 612.8
• DOI: 10.1016/j.ijdevneu.2017.03.011
• Languages: English
• ISSNs: 0736-5748

Abstract

Highlights: Mice exposed to HFD showed reduced performance on Morris Water Maze. Peripheral insulin resistance exacerbates HFD induced cognitive deficits. Mechanisms converge on decreased hippocampal signaling, which alters memory. Abstract: There is growing evidence that over consumption of high-fat foods and insulin resistance may alter hippocampal-dependent cognitive function. To study the individual contributions of diet and peripheral insulin resistance to learning and memory, we used a transgenic mouse line that overexpresses ecto-nucleotide pyrophosphatase phosphodiesterase-1 in adipocytes, which inhibits the insulin receptor. Here, we demonstrate that a model of peripheral insulin resistance exacerbates high-fat diet induced deficits in performance on the Morris Water Maze task. This finding was then reviewed in the context of the greater literature to explore potential mechanisms including triglyceride storage, adiponectin, lipid composition, insulin signaling, oxidative stress, and hippocampal signaling. Together, these findings further our understanding of the complex relationship among peripheral insulin resistance, diet and memory.